The Timing of the Circadian Clock and Sleep Differ between Napping and Non-Napping Toddlers.

The Timing of the Circadian Clock and Sleep Differ between Napping and Non-Napping Toddlers.
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DOI:
10.1371/journal.pone.0125181
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发表时间:
2015
期刊:
影响因子:
3.7
通讯作者:
LeBourgeois MK
LeBourgeois MK
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Akacem LD;Simpkin CT;Carskadon MA;Wright KP Jr;Jenni OG;Achermann P;LeBourgeois MK

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内部生物钟的时间安排在整个生命周期中显示出巨大的个体间差异。尽管大多数幼儿的睡眠-觉醒模式包括下午小睡,但小睡与幼儿时期昼夜节律阶段之间的关联仍未被探索。这项研究检查了小睡和不小睡的幼儿之间昼夜节律阶段和睡眠的差异。收集了 20 名幼儿(34.2±2.0 个月;12 名女性;15 名午睡者)的数据。儿童遵循习惯性小睡和非小睡睡眠时间表(通过体动记录仪监测)5 天,然后进行家庭唾液弱光褪黑激素发作 (DLMO) 评估。平均而言,在 DLMO 评估前 5 天中,午睡儿童有 3.6±1.2 天在午睡机会期间入睡。对于这些小睡的儿童,褪黑激素开始分泌的时间晚了 38 分钟(p = 0.044;d = 0.93),活动记录估计的就寝时间晚了 43 分钟(p = 0.014;d = 1.24),睡眠开始时间晚了 59 分钟(p = 0.006;d = 1.46),睡眠开始潜伏期延长了 16 分钟。 (p = 0.030; d = 1.03) 高于不午睡的人。睡眠中和醒来的时间并没有因小睡状态而有所不同。与 DLMO 的就寝时间、入睡时间或睡眠中相关系没有观察到差异;然而,小睡幼儿的唤醒时间相位差要小 47 分钟(p = 0.029;d = 1.23)。平均而言,与不午睡的人相比,午睡的人夜间睡眠时间短 69 分钟(p = 0.006;d = 1.47),在床上的时间短 49 分钟(p = 0.019;d = 1.16)。午睡天数与褪黑激素的起始时间相关(r = 0.49;p = 0.014)。我们的研究结果表明,午睡会影响幼儿时期褪黑激素开始时间的个体差异。幼儿小睡的延迟就寝时间可能会导致晚上晚些时候接触光线,从而延迟生物钟和睡眠的时间。昼夜节律阶段的早期发育轨迹是否涉及与午睡减少相关的提前是一个需要纵向数据的问题,因为儿童从双相睡眠-觉醒模式转变为单相睡眠-觉醒模式。
The timing of the internal circadian clock shows large inter-individual variability across the lifespan. Although the sleep-wakefulness pattern of most toddlers includes an afternoon nap, the association between napping and circadian phase in early childhood remains unexplored. This study examined differences in circadian phase and sleep between napping and non-napping toddlers. Data were collected on 20 toddlers (34.2±2.0 months; 12 females; 15 nappers). Children followed their habitual napping and non-napping sleep schedules (monitored with actigraphy) for 5 days before an in-home salivary dim light melatonin onset (DLMO) assessment. On average, napping children fell asleep during their nap opportunities on 3.6±1.2 of the 5 days before the DLMO assessment. For these napping children, melatonin onset time was 38 min later (p = 0.044; d = 0.93), actigraphically-estimated bedtime was 43 min later (p = 0.014; d = 1.24), sleep onset time was 59 min later (p = 0.006; d = 1.46), and sleep onset latency was 16 min longer (p = 0.030; d = 1.03) than those not napping. Midsleep and wake time did not differ by napping status. No difference was observed in the bedtime, sleep onset, or midsleep phase relationships with DLMO; however, the wake time phase difference was 47 min smaller for napping toddlers (p = 0.029; d = 1.23). On average, nappers had 69 min shorter nighttime sleep durations (p = 0.006; d = 1.47) and spent 49 min less time in bed (p = 0.019; d = 1.16) than non-nappers. Number of days napping was correlated with melatonin onset time (r = 0.49; p = 0.014). Our findings indicate that napping influences individual variability in melatonin onset time in early childhood. The delayed bedtimes of napping toddlers likely permits light exposure later in the evening, thereby delaying the timing of the clock and sleep. Whether the early developmental trajectory of circadian phase involves an advance associated with the decline in napping is a question necessitating longitudinal data as children transition from a biphasic to monophasic sleep-wakefulness pattern.
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